Evidence map›Paper›PMID 38720166›Full record

ArticlePhysiological reports2024

Plausible role of INPP4A dysregulation in idiopathic pulmonary fibrosis.

Meghana Arvind, Bijay Pattnaik, Atish Gheware, Y S Prakash, Mousami Srivastava, Anurag Agrawal, Naveen Kumar Bhatraju

Abstract read
In one paragraph

Article in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Meghana ArvindCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Bijay PattnaikCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Atish GhewareCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Y S PrakashDepartment of Anaesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Mousami SrivastavaCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Anurag AgrawalCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.
Naveen Kumar BhatrajuCentre of Excellence for Translational Research In Asthma and Lung diseases (TRIAL), CSIR-Institute of Genomics and Integrative Biology, New Delhi, India.ORCID 0000-0002-6248-7956

Funding

Neurotrophins in the LungR01HL088029 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S. · 2009 to 2022
$5.9M
Nicotine, Airway Smooth Muscle and AsthmaR01HL142061 · NHLBI · MAYO CLINIC ROCHESTER · PI PABELICK, CHRISTINA MARIA, PRAKASH, Y. S. · 2019 to 2022
$2.0M
NHLBI NIH HHS R01 HL088029NHLBI NIH HHS R01 HL142061
6 · The paper itself

Abstract

INPP4A has been shown to be involved in the regulation of cell proliferation and apoptosis of multiple cell types including fibroblasts. Previous reports from our group have demonstrated the role of inositol polyphosphate 4-phosphatase Type I A (INPP4A) in these functions. Though existing evidences suggest a critical role for INPP4A in the maintenance of lung homeostasis, its role in chronic lung diseases is relatively under explored. In the current study, we made an attempt to understand the regulation of INPP4A in idiopathic pulmonary fibrosis (IPF). Through integration of relevant INPP4A gene expression data from public repositories with our results from in vitro experiments and mouse models, we show that INPP4A is altered in IPF. Interestingly, the direction of the change is dependent both on the disease stage and the region of the lung used. INPP4A was found to be upregulated when analyzed in lung sample representative of the whole lung, but was downregulated in the fibrotic regions of the lung. Similarly, INPP4A was found to be high, compared to controls, only in the early stage of the disease. Though the observed increase in INPP4A was found to be negatively correlated to physiological indices, FVC, and DL

Indexed as

Idiopathic Pulmonary FibrosisPhosphoric Monoester HydrolasesAnimalsFemaleFibroblastsHumansLungMaleMiceMice, Inbred C57BLphosphatidylinositol-3,4-bisphosphate 4-phosphatasePhosphoric Monoester Hydrolasesbleomycindisease heterogeneityidiopathic pulmonary fibrosisINPP4Atransforming growth factor‐β

Identifiers

PMID38720166
PMCPMC11078778

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.